OBJECTIVE: To investigate the effects of electroacupuncture(EA) at Taichong(LR 3) and Baihui(DU 20)on myocardial hypertrophy in spontaneously hypertensive rats(SHRs).METHODS: Thirty-six SHRs were randomly assigned to ...OBJECTIVE: To investigate the effects of electroacupuncture(EA) at Taichong(LR 3) and Baihui(DU 20)on myocardial hypertrophy in spontaneously hypertensive rats(SHRs).METHODS: Thirty-six SHRs were randomly assigned to model, EA, and Losartan groups, with twelve rats per group. Twelve Wistar Kyoto rats were selected as the normal control group. Systolic blood pressure(SBP) and cardiac function were measured in all rats.Expression levels of factors associated with the phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin(PI3K/Akt/mTOR) pathway were evaluated by Western blotting and real-time PCR.Pathological changes of the heart tissue were observed by hematoxylin-eosin staining.RESULTS: After treatment, enhanced SBP was significantly decreased in the EA and Losartan groups compared with the model group(P < 0.01). Echocardiographic and morphological analyses revealed that enhanced end-diastolic interventricular septal thickness and left ventricular posterior wall thickness, as well as ratio of left ventricular weight to body weight were markedly diminished in the EA and Losartan groups(P < 0.01 or P < 0.05), while reduced left ventricular end-diastolic dimension and left ventricular ejection fraction were significantly ameliorated(P < 0.01). Real-time PCR and western blotting analyses showed that the expression levels of PI3K,Akt, and mT OR in SHRs were significantly up-regulated by EA and Losartan(P < 0.01), while the expression levels of PTEN and ANP were down-regulated(P < 0.01).CONCLUSION: EA at Taichong(LR 3) and Baihui(DU20) inhibited the development of cardiac hypertrophy and improved the cardiac function in SHRs, possibly through regulation of the PI3K/Akt/mTOR signalling pathway.展开更多
目的研究右旋美托咪啶(dexmedetomidine,Dex)对异氟醚所致新生大鼠海马细胞凋亡的保护作用及与Akt/Bad信号通路的关系。方法出生7 d SD大鼠随机分为空气组(Air+NS)、二甲基亚砜组(Air+DMSO)、LY294002组(Air+LY)、异氟醚组(Iso+NS)、异...目的研究右旋美托咪啶(dexmedetomidine,Dex)对异氟醚所致新生大鼠海马细胞凋亡的保护作用及与Akt/Bad信号通路的关系。方法出生7 d SD大鼠随机分为空气组(Air+NS)、二甲基亚砜组(Air+DMSO)、LY294002组(Air+LY)、异氟醚组(Iso+NS)、异氟醚+Dex组(Iso+Dex)、异氟醚+Dex+LY294002组(Iso+Dex+LY)。前3组吸入空气6h,后3组吸入体积分数为0.0075异氟醚6h。吸入异氟醚前40min,Air+DMSO组、Air+LY组和Iso+Dex+LY组分别经侧脑室注射5μl体积分数为0.1的DMSO或25μg LY294002;Iso+Dex组和Iso+Dex+LY组分别在麻醉0、2、4 h腹腔内注射Dex 25μg·kg-1;Air+NS组和Iso+NS组在同时间点腹腔内注射等体积生理盐水。Western blot法检测海马激活型caspase-3、Akt、磷酸化Akt(p-Akt)、Bad、磷酸化Bad(p-Bad)、Bcl-xl蛋白表达变化(n=5),TUNEL法检测海马CA1区细胞凋亡(n=5)。结果 Dex可明显减少异氟醚引起的海马CA1区TUNEL阳性细胞表达(P<0.01),减低激活型caspase-3(P<0.01)和Bad蛋白表达(P<0.01),上调p-Akt/Akt、p-Bad/Bad和Bcl-xl/Bad比值(P<0.01)。LY294002逆转了Dex对上述蛋白表达的影响。结论Dex通过激活Akt/Bad信号通路减少异氟醚诱导的新生大鼠海马细胞凋亡。展开更多
基金Supported by Beijing Natural Science Foundation:Regulating effect of electroacupuncture on cardiac hypertrophy of spontaneously hypertensive rats based on PI3K/AKT signal transduction pathway(No.7162121)Young Teacher Program of Beijing University of Chinese Medicine:Mechanism of acupuncture on left ventricular remodeling in spontaneously hypertensive rats based on microRNA-195 targeting TGF/Smads signaling pathway(No.2017-JYB-JS-030)
文摘OBJECTIVE: To investigate the effects of electroacupuncture(EA) at Taichong(LR 3) and Baihui(DU 20)on myocardial hypertrophy in spontaneously hypertensive rats(SHRs).METHODS: Thirty-six SHRs were randomly assigned to model, EA, and Losartan groups, with twelve rats per group. Twelve Wistar Kyoto rats were selected as the normal control group. Systolic blood pressure(SBP) and cardiac function were measured in all rats.Expression levels of factors associated with the phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin(PI3K/Akt/mTOR) pathway were evaluated by Western blotting and real-time PCR.Pathological changes of the heart tissue were observed by hematoxylin-eosin staining.RESULTS: After treatment, enhanced SBP was significantly decreased in the EA and Losartan groups compared with the model group(P < 0.01). Echocardiographic and morphological analyses revealed that enhanced end-diastolic interventricular septal thickness and left ventricular posterior wall thickness, as well as ratio of left ventricular weight to body weight were markedly diminished in the EA and Losartan groups(P < 0.01 or P < 0.05), while reduced left ventricular end-diastolic dimension and left ventricular ejection fraction were significantly ameliorated(P < 0.01). Real-time PCR and western blotting analyses showed that the expression levels of PI3K,Akt, and mT OR in SHRs were significantly up-regulated by EA and Losartan(P < 0.01), while the expression levels of PTEN and ANP were down-regulated(P < 0.01).CONCLUSION: EA at Taichong(LR 3) and Baihui(DU20) inhibited the development of cardiac hypertrophy and improved the cardiac function in SHRs, possibly through regulation of the PI3K/Akt/mTOR signalling pathway.
